We have a lot of control of our day to day lives; we get to choose where we go, who we see, and what we eat. But those decisions are often shaped by unseen forces, including some right under our noses (and all over our bodies for that matter). Scientists working with E. coli bacteria in mice say a taste for sweets might literally come from our guts. They present their findings this week in Florida at the annual meeting of the Association for Chemoreception Sciences.
Some of the bacteria on our bodies are a force for good: they help us digest our food and stay healthy. Some are less helpful. Science is really just beginning to discover the many ways we interact with our bacteria. Some of our choices, like smoking, eating a low-fiber diet, or using deodorant, affect our bacteria. But the reverse may also be true: our bacteria could affect our choices.
This all has to do with the fact that these tiny organisms get hungry. Those in your digestive tract have it pretty easy: They just chow down on the food you shove in there. Some prefer fats, while others thrive on sugar. And if there are enough of them, what they want may become what you want.
“In our field, we are starting to think about how hormones and different factors affect the taste system, even at the level of taste buds, and contribute to obesity,” presenter Lynnette McCluskey said in a press statement. McCluskey is a neuroscientist at Augusta University's Medical College of Georgia. "Identifying the taste, whether it's sweet or not, is the first step in feeding. We wanted to know if you change the environment in the gut, what happens to the taste system."
McCluskey and her colleagues had previously found that they could reduce a mouse’s ability to identify sweet tastes by dropping a molecule called lipopolysaccharide (LPS) on its tongue. The LPS was extracted from the cell wall of E. coli bacteria, then detoxified so the mice would not get sick.
For this experiment, the researchers wanted to find out if actually ingesting LPS could actually make mice lose interest in sweet flavors. They implanted small doses of detoxified LPS in each mouse’s gut, then offered them access to four sweeteners: glucose, sucrose (table sugar), saccharin (a.k.a. Sweet’n Low), and acesulfame potassium (a.k.a. Sweet One).
Within 15 hours, mice dosed with LPS had higher levels of a hormone called leptin, which tells us when to stop eating. One week later, those mice had lost their preference for sweets. Even the number of sweet taste receptors on their tongues had decreased. It wasn’t that they’d lost their appetites altogether; the mice were still healthy and ate other food as they had before. It was just that sugar had lost its appeal. Yet seven days later, the rodents’ taste for sweetness had returned.
The researchers were left with a number of questions. How did LPS in the gut cause a mouse’s body to make more leptin? Why did it take seven days to kick in? Why did it stop? And why leptin? "There may be other gut hormones involved as well,” said McCluskey, “but we know that leptin works.”